|Causes and Consequences of Intrauterine Growth Retardation, Proceedings of an IDECG workshop, November 1996, Baton Rouge, USA, Supplement of the European Journal of Clinical Nutrition (International Dietary Energy Consultative Group - IDECG, 1996, 100 pages)|
|Neurodevelopmental outcome of small-for-gestational-age infants|
Cerebral palsy is found in 1 to 2 per 1000 children. It has been well known for nearly 150 years that low birthweight infants are at greater risk for this outcome than more average size infants are. However, it has only been in the last 40 years that a relatively clear distinction has been made between babies born preterm and those born small for gestational age, whether born at term or preterm. As emphasized above, the boundaries between SGA and AGA are not well defined, and have shifted over time. The incidence of cerebral palsy is highly dependent on gestational age at birth, ranging from as high as 250/1000 for infants born at 23 or 24 weeks to 30/1000 at 30 weeks, to 5/1000 at 36 weeks, to 1/1000 for infants born at 40 weeks (Escobar et al, 1991). It is therefore important to define the impact of SGA on cerebral palsy against this background. In doing so, it becomes very obvious that evaluating the relationship between SGA and cerebral palsy in term infants requires huge sample sizes and the answer is not likely to be elucidated by relatively small prospective cohort studies.
We should also emphasize that the composition of the preterm population is changing, especially as more and more very low birthweight infants are surviving. In addition, the preterm population consists of infants that are not only preterm, but SGA as well. The outcome for these latter infants may be different than for infants who are only preterm.
Despite these considerations, review of the available data regarding the relationship between SGA and cerebral palsy does allow us to reach some conclusions. As an example, babies born at term and later diagnosed with cerebral palsy tend to be lighter at birth than those who are not diagnosed as having cerebral palsy (Ellenberg and Nelson, 1979; Blair and Stanley, 1990). Nevertheless, most small babies, even if they are very SGA, do not end up with cerebral palsy, and most children with cerebral palsy are of normal birthweight. Translated into a measure of risk, being SGA at term appears to double or triple the risk of cerebral palsy, i.e. from 1 or 2 per 1000 live births to 2 to 6 per 1000 live births. Factors that appear to be associated with increased risk are the severity of the SGA, male sex, and whether asphyxia or other risk factors for cerebral palsy were present.
In many studies of preterm infants and cerebral palsy, preterm SGA infants appear to have less cerebral palsy than AGA preterm infants (Hack et al, 1989; Robertson et al, 1990; Saigal et al, 1990; Sung et al, 1993). These SGA preterm infants are frequently born in conjunction with maternal preeclampsia, and most studies suggest a protective effect against cerebral palsy of preeclampsia in preterm SGA infants. However, even this conclusion is not unanimous. Robertson et al (1990), for example, studying £1500 g, less than tenth percentile infants, found that preterm SGA infants were not at greater risk to be disabled with cerebral palsy than were AGA birthweight or gestational age matched controls, but all were at substantially greater risk than a term AGA comparison group. On the other hand, Hack et al (1989), studying £ 1500 g infants, observed an 8% rate of cerebral palsy in the AGA group, but only a 3% rate (p <.01) in the SGA group. Veelken et al, also showed that < 1500 g SGA infants had less cerebral palsy than < 1500 g preterm AGA infants (Veelken et al, 1992). We interpret these data to indicate that in cohorts defined by birthweight, SGA infants have less cerebral palsy. However, in cohorts defined by gestational age, SGA infants had similar or higher rates of cerebral palsy.